Staphylococcal Chromosomal Cassette mec Type I, spa Type, and Expression of Pls Are Determinants of Reduced Cellular Invasiveness of Methicillin‐Resistant Staphylococcus aureus Isolates
1Institute of Medical Microbiology and 2Institute for Hygiene, University Hospital of Münster, Germany; 3Department of Biological and Environmental Sciences, General Microbiology, and 4Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, and 5Division of Clinical Microbiology, Helsinki University Central Hospital (HUCH) Laboratory Diagnostics, HUCH, Helsinki, Finland
We have shown previously that pls, which codes for the surface protein Pls of methicillin‐resistant Staphylococcus aureus (MRSA), reduces adhesion to immobilized fibronectin, fibrinogen, laminin, and immunoglobulin G as well as invasion of host cells. Here, we tested a collection of 66 clinical MRSA isolates—48 negative for pls/Pls (pls−/Pls−), 15 positive for pls/Pls (pls+/Pls+), and 3 harboring the pls gene but not expressing Pls (pls+/Pls−)—for cellular invasiveness. Invasion of 293 cells by pls+/Pls+ strains was lower than that by the pls−/Pls− strains (median [range], 36% [22%–70%] vs. 93% [25%–162%]). The 3 pls+/Pls− strains (median [range], 95% [63%–103%]) were as invasive as the pls−/Pls− strains. In addition, we identified a pls+/Pls+ staphylococcal chromosomal cassette mec (SCCmec) IV strain. In conclusion, 3 properties—pls/Pls, SCCmec type, and spa type—strongly predicted the cellular invasiveness of MRSA strains, as indicated by good clustering. In contrast, the spa type–deduced multilocus sequence typing clonal complex (MLST‐CC) was not able to predict the invasiveness of MRSA strains equally well. The underlying mechanism remains to be elucidated.
Received 21 August 2006; accepted 29 December 2006; electronically published 23 April 2007.
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Online publication date: 1-Jul-2009.
Online publication date: 1-Mar-2009.
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Potential conflicts of interest: none reported.
Presented in part: 10th International Symposium on Staphylococci and Staphylococcal Diseases, Charleston, South Carolina, 23–27 October 2004 (poster PA‐34); 56th Annual Meeting of the German Society for Hygiene and Microbiology, Münster, Germany, 26–29 September 2004 (poster MPP005).
Financial support: This work was supported by the Deutsche Forschungsgemeinschaft (Collaborative Research Center 492, project B9), in part by grant Si2/039/06 from the Interdisciplinary Center for Clinical Research (IZKF Münster), by a grant from the Academy of Finland (project 1206356), and by a grant from Bundesministerium für Bildung und Forschung, Germany (Pathogenomic Plus Network PTJ‐BIO/0313801B).
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Present affiliation: Institute of Hygiene and Microbiology, University of Würzburg, Würzburg, Germany.





